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Management of the Medically Compromised Patient

Management of the Medically Compromised Patient

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Management of the Medically Compromised Patient

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  1. Management of the Medically Compromised Patient Erica Phillips July 6, 2012

  2. What we’ll cover today . . . • Hemophilia • Hepatitis • Sickle Cell Anemia • HIV/AIDS • Leukemia

  3. Goals of Treatment • Achieve optimal oral health for patient. • Develop a working relationship with patient’s PCP. • Minimize complications. • Aggressive prevention. 

  4. Hemophilia • a disorder of hemostasis resulting from a deficiency of a procoagulation factor. • X-linked recessive affecting 1/7500 males. Female carriers may have low baseline activity and should be evaluated before dental tx. Hemophilia A: -Factor VIII deficiency (Antihemophilic Factor) -most common type. Hemophilia B (Christmas Disease): -Factor IX deficiency -1/4 as prevalent as Hemophilia A. Hemophilia C: -Factor XI deficiency or Rosenthal’s disease. -autosomal recessive trait. M=F. -Ashkenazi Jews most often affected. Other deficiencies( II, V, VII and XIII ) are rare and autosomal recessive.

  5. Coagulation Cascade

  6. Hemophilia A & B: Severity

  7. Hemophilia Treatment: Replacement of Deficient Factor Hemophilia A: • For routine hemorrhaging in joints, soft tissues or oral bleeding, a one time correction of 40-50% Factor VIII will stop bleeding. • Desmopressin: DDAVP (1-deamino-8-D-arginine vasopressin) is a synthetic analogue of vasopressin used for minor hemorrhagic episodes. Causes increase in Factor VIII and VWF. • Caution with DDAVP: long-term use can cause tachyphylaxis. May also be associated with hyponatremia, water retention, and seizures (must monitor electroytes). Hemophilia B: • Minimum of 40% correction of purified Factor IX concentrate.

  8. Hemophilia: Administration of Treatment • Clotting factor is measured in International Activity Units. • Regimen depends on severity of disease, number of bleeding episodes, and physician’s recommendations. • Therapy is either “on-demand” (after a bleeding episode) or prophylactic at regularly scheduled intervals. • Prophylactic treatment is standard of care for those with severe hemophilia. • If pt has catheter placed for venous access, may consider antibiotic therapy (not currently recommended by CDC).

  9. Von Willebrand Disease • abnormal VWF (either quantity or quality) in plasma, platelets, megakaryocytes and endothelial cells. • important for platelet adhesion to subendothelium via collagen(formation of platelet plug). • Symptoms include: • Bleeding from skin and mucosa • Bruising • Epistaxis • prolonged bleeding after surgery • Menorrhagia Tx: DDAVP. If no response, may try exogenous VWFconcentrate.

  10. Von Willebrand Factor

  11. Treatment of Hemophilia:Complicating Factors • Inhibitors: antibodies that neutralize the coagulation factor administered. • Low-responders have peak levels of inhibitors <5 Bethesda Units. Treat with factor concentrate. • High responders have peak titers >5 BU and require bypassing products (prothrombin complex concentrate or recombinant factor VIIa). • Arthritis and degenerative joint disease secondary to recurrent bleeding. • Blood-borne viral infection (b/c of blood or blood products used in tx), especially HBV and HCV.

  12. Hemophilia: Dental Management • Important for Med Hx: type of disorder, severity, frequency and tx of episodes, and inhibitor status. • Notice unusual bleeding! As the patient’s dentist, you may be the first to make the diagnosis. Mouth lacerations and persistent oral bleeding are commonin children. • Dental providers should schedule evaluations and interventions on planned infusion days. • Those treated with on-demand regimens require planning for replacement therapy in preparation for specific procedures. Effort should be made to do as much as possible in one appointment to avoid multiple costly infusions. • Discussion with hematologist: type of anesthetic to be used, invasiveness of procedure, amount of bleeding anticipated, time involved in oral wound healing. • Pharmacological Management

  13. Adjunctive Pharmacological Management for Dental Services Antifibrinolyticagents: • prevent clot lysis in oral cavity. • Aminocaproic acid (Amicar) and Tranexamic Acid (Cyklokapron). • Taken orally immediately before dental treatment and then every 6-8 hours for approximately one week. • Side effects of antifibrinolytics: headache, nausea, dry mouth. May increase risk of thrombosis in those with renal or urinary tract bleeding, evidence of DIC or prolonged use of replacement therapy in high responders.

  14. Pain Control for Hemophiliacs: • Sedation, nitrous oxide and hypnotics for anxiety. • Avoid aspirin or Ibuprofen. Use acetaminophen (Tylenol) for acute pain. Narcotics may be required for severe pain. • IM injections are contraindicated b/c of risk of hematoma. • PDL injections okay if factor replacement being given. • If no replacement therapy or anti-fibrinolytic agents, can still infiltrate. For highly vascular areas, replacement levels should be at least 30-40%. • Blocks: caution required. The IAN and PSAN are surrounded by loose, connective, highly vascularized tissue. • Can get dissecting hematoma, may cause airway obstruction and a life-threatening bleed. • Requirement is minimum of 40% factor correction with blocks. • Must aspirate! If blood in aspirate, may need to give further give factor replacement and must notify hematologist immediately after procedure.

  15. Hemophilia & Dental Procedures • Prevention: • OHI, brushing, flossing, topical fluoride, systemic fluoride, dietary counseling, professional exams. • Rubber cup prophy and supragingival scaling can be done without replacement therapy. • Control minor bleeds with moistened gauze pressure, topical bovine thrombin, microfibrillarcollagen, local fibrin glue. • Periodontal Tx: • Initial supragingival scaling followed by 1-2 week healing period so that gingival edema/hyperemia will decrease. • Then can remove calculus and irritants with less bleeding. • Subgingival scaling: consider replacement therapy, depending on amount of bleeding expected and severity of deficiency.

  16. Hemophilia & Dental Procedures • Restorative: • Thin rubber dam essential for isolation and to protect soft tissues from laceration. Avoid lacerating the gingiva with the clamp or frame. • Can use wedges and matrix bands as normal (wedge protects the papilla). • Caution with high speed suction and intraoral radiographs to avoid sublingual bleeds. • Pulpal therapy: • Indirect pulp cap to avoid exposure. If exposure occurs, can use cotton pellet to control bleeding. • Pulpotomy or pulpectomy is preferable to extraction.

  17. Hemophilia & Extractions: Simple exo of erupted permanent teeth and multirooted primary teeth: • 30-40% factor correction within 1 hour of dental tx. • Antifibrinolytictx immediately before or after procedure and continues for 5-10 days. • Clear liquid diet for first 72 hours, then soft pureed diet for a week. . At day 10 can start normal diet. • No straws, metal utensils, pacifiers or bottles. Surgical exo of impacted, partially erupted or unerupted teeth: • higher factor activity level targeted. May want factor replacement post op. • antifibrinolytictherapy started immediately before or after procedure, continue for 7-10 days.

  18. Hemophilia & Extractions: Simple exo of single rooted primary teeth: • evaluate root development to decide if replacement therapy required. • If only partially formed root, antifibrinolyticplus local hemostatic agents may be enough. Bleeding from exfoliation of primary teeth: • direct finger and gauze pressure for several minutes. Topical agents. • Antifibrinolytics if bleeding slow and continuously. • Rarely need RT, usually when gingival tissue is repeatedly traumatized during exfoliation.

  19. Hemophilia & Extractions: Local hemostasis after exo: • topical hemostatic agents: thrombin, microfibrillarcollagen, or fibrin glue on wound. • Direct pressure with gauze. • Stomadhesive dressing protects from oral environment. • Avoid sutures, unless they will really enhance healing and in this case, use resorbable kind.

  20. Hemophilia & Extractions: Surgical complications: • bleeds may occur 3-4 days post op when clot breaks down. • Typical clot is dark red, protrudes from surgical site, covering several teeth. • Abnormal clot should be removed after RT given, area cleaned to isolate source of bleed, repack and use AF agents.

  21. Hemophilia and Orthodontics: • early intervention can help prevent need for more complex tx later on. • Interceptive or full-banded ortho can be done. • Avoid sharp edges and wires when placing and adapting bands. • Preformed bands and brackets can bond directly to teeth and avoid contact with gingiva. Use longer-acting wires and springs b/c needs less adjusting. • oral hygiene very important to avoid inflammation of gingiva. Water irrigating device helpful for homecare.

  22. Viral Hepatitis • Infection that produces inflammation of liver cells. • Most cases resolve after acute infection, esp A and E. • Prodromal (early phase): lethargy, loss of appetite, nausea, vomiting, abdominal pain, jaundice, hepatomegaly or splenomegaly. • Jaundice is clinically apparent when bilirubin levels in plasma are >2.5mg/100 mL). • Convalescent phase: symptoms disappear, hepatomegaly and abnormal liver function may persist for up to four months. • > 4 million Americans are chronic virus carriers(low levels of the virus > 6 months). • Can become chronic active virus after decades, leading to hepatocellular necrosis. • In those with chronic active hepatitis, 20% get cirrhosis, and 1-5% develop a primary hepatocellular carcinoma.

  23. Functions of the Liver • Bile secretion (fat absorption) • Converts sugar to glycogen • Excretes bilirubin (waste product of hemoglobin). • Synthesis of coagulation factors • Drug metabolism When impaired: look out for bleeding issues and impaired drug metabolism!

  24. HAV • Between 125,000 and 200,000 new cases of Hep A occur annually in U.S. (47% of acute hepatitis cases reported). • Picornavirus – RNA virus that replicates in liver, excreted in bile and shed in stool. Spread by fecal-oral route. • Common sources are contaminated water, restaurants, raw shellfish, daycare centers. • May present as acute fever with jaundice, anorexia, nausea, malaise, lymphadenopathy, night sweats. • 10% are asymptomatic. • Infants and children will present with mild non-specific symptoms without jaundice. • no carrier state. • IgG or IgManti-HAV indicates past infection and lifelong immunity to HAV. • Vaccine (inactivated virus) available since 1996 in the U.S. Can also give HAV Ig within 2 weeks of exposure.

  25. HBV • 140,000-320,000 reported annually in U.S. (27% of acute Hep infections). • Hepadnavirus -replicates in hepatocytes and stem cells. Transmitted by parenteral, percutaneous or mucous membrane inoculation. Vertical transmission from mom to baby possible. • Most infections occur in young adults. 10% occur in infants and young children. • 70-90% are asymptomatic in acute phase. • Chronic HBV develops in over 25% carriers. Can progress to cirhossis or liver cancer. • Lab tests: Antibody to HebB surface antigen: indicates resolution of natural infection or successful vaccination(long term immunity). Antibody to core antigen (IgG or IgM anti-HBc): indicates recent infection. Anbitbody to HepBe antigen (“early” antigen from cleavage of core antigen) indicates infectivity. • Recombinant DNA vaccine recommended for healthcare workers. Universal vaccination of infants. Post exposure immunoprophylaxis of infants born to HBsAg-positive women. Hep D • Fulminant hepatitis when infection coexists with HepB. (Requires Hep B outer coat proteins) to superinfect.

  26. HCV • The most common bloodborne infection in the U.S. 3.5-4 million Americans have chronic infection. • Flavivirus– parenterally transmitted. • Vertical transmission from mother to child possible: accounts for 5% of HCV cases. • 60-70% asymptomatic in acute phase. • 70-85% develop chronic hepatitis. • No immunization available. • leading cause of liver transplants in U.S. • Dx: anti-HCV in serum.

  27. Hepatitis Tx Acute phase: • bed rest, fluids, nutritious high calorie diet. • No alcohol or drugs that are metabolized by liver. • Monitor viral antigens and ALT levels for 6 months to test whether infection has resolved. Chronic hepatitis: • Interferon (IFN) alpha-2b, 3x/week for 6 months -1 year. Can normalize ALT levels and lower risk of hepatocellular carcinoma Only 10-30% achieve long term remission. • Lamivudine (nucleoside analog active against HBV) or ribavirin (against HCV). • Corticosteroids for fulminant infection. • Liver transplant for cirrhosis.

  28. Oral Manifestations of Hepatitis • Abnormal bleeding: abnormal clotting factor synthesis, inadequate fibrin stabilization, excessive fibrinolysis, thrombocytopenia. • Rarely, hepatocellular carcinoma will metastasize to jaw. Will present as hemorrhagic expanding masses in premolar and ramus areas of mandible.

  29. Dental Management of Hepatitis: For pts with active hepatitis: • Urgent (absolutely necessary) dental work only. • Minimize aerosols and avoid drugs that are metabolized in liver. • For surgery: preopprothrombin time and bleeding time should be obtained. Obtain platelet count, confirm that INR is under 3.5. For pts who are carriers: • Standard universal precautions • Consult with physicians: liver function lab tests to assess hemostasis issues and metabolic problems. • No elective tx if signs or symptoms of hepatitis. Refer to physician. • If recovered, no tx modifications necessary

  30. Drugs metabolized primarily by liver: • Local Anesthetics: Lidocaine (xylocaine), mepivicaine (carbocaine), prilocaine (citanest), Bupivicaine (marcaine). • Analgesics: Aspririn, Acetominophen, Codeine, Ibuprofen, Meperidine. • Sedatives: Diazepam, Barbiturates. • Antibiotics: Ampicillin, Tetracycline, Metronidazole, Vancomycin. May be used unless hepatic disease is severe, but in limited amounts Diminished dosages should be considered when: • aminotransferases > 4x normal • Serum bilirubin > 35 μM/L or 2 mg/dL. • Serum albumin levels < 35 mg/L • Signs of ascitiesand encephalophathy, prolonged bleeding time.

  31. Sickle Cell Anemia • Autosomal recessive • More common in those of African descentand also Italians, Middle Eastern, Greek and Indians. The mutation confers advantage against infection with P. falciparum (malaria). • 1/600 African Americans have sickle cell anemia. • Valine for glutamic acid substitution in beta chain of Hemoglobin forms Hemoglobin S instead of HbA  decreased oxygen capacity, cell rigidity and membrane damage and sickling of cells under lower oxygen tension. • Results in erythrostasis, increased blood viscosity, reduced blood flow, hypoxia, vascular occlusion. • Clinical signs include jaundice, pallor, dactylitis, leg ulcers, organomegaly, cardiac failure, ocular damage, stroke, bone pain, abdominal pain, delays in growth and development.

  32. Sickle Cell Crisis: • Precipitated by acidosis, hypoxia, hypothermia, hypotension, stress, hypovolemia, dehydration,trauma,fever and infection. • decreased RBC production  severe joint and abdominal pain, fever, ischemia and infarction of organs. • Deterioration of cardiac, pulmonary and renal fxn.

  33. Oral Manifestations of SCA: • Radiographic changes: • generalized radiolucencies. • loss of trabeculation, more prominent lamellar striations. “stepladder” appearance of bone b/t teeth. • prominent lamina dura • Hyperplasia of marrow spacesbecause of increased erythropoetic demands. • Generalized osteoporosis of mandible – thinning of inferior border. • Frontal bossing and “hair on end” appearance of cortical regions of skull radiographs. • Retrusion of mandible due to decreased bone growth. • Hypomineralized teethor delayed eruption of teeth. • Infarcts in jawdue to vaso-occlusion: osteomyelitis, pulpal necrosis, ischemic necrosis in mandible, and peripheral neuropathy( Dental pain with no pathology). • Pale oral mucosa • Jaundice (from excessive erythrocyte destruction leading to hyperbilirubinemia).

  34. “Hair on End” Enlarged marrow spaces

  35. Medical Management of SCA: • Daily folic acid supplements to prevent crisis. • Penicillin prophylaxis for first 5 years of life. • Hydroxyurea +/- erythropoietin to induce formation of HbF (and prevent HbS). When crisis occurs: • High doses of folic acid • Analgesics • Hydration • Blood transfusions. Bone Marrow Transplantation: moderate success in treating SCA (25%) but increased mortality.

  36. Dental Management of SCA: • Can receive routine dental care during non-crisis periods. During a sickle cell crisis, emergency tx only. • Short appointments to lower stress. Avoid long/complicated procedures. • Aggressive prevention to lower chance of infection, especially when patient has spleen defects. • Currently a debate over need for prophylactic abx. Avoid tissue irritation leading to bacteremias. For major surgical procedures: prophylactic penicillin to prevent wound infection or osteomyelitis. • Restoration of teeth is preferable to exo. Pulpectomyokay as long as tooth is noninfected. If infected and persistent, extract. • OHI essential. • Orthodontics may be helpful for skeletal changes. Careful monitoring required. • Use of epinephrine is controversial (some believe it may impair blood flow and cause vascular occlusion). • Use of nitrous oxide okay. Avoid diffusion hypoxia at end of procedure. At least 50% oxygen should be provided. • Avoid dehydration – fluid intake important, esp during IV sedation. • Pain control: acetaminophen and small doses of codeine are acceptable. Avoid aspirin (salicylates) in high doses b/c acid effect may cause crisis. • IV sedation: caution required. Avoid barbiturates and narcotics (supress respiratory center). Can use Diazepam. • GA : if Hb< 7g/dL and hematocrit <20%, transfusion may be required. • Pedspts are less likely to have post-transfusion complications.

  37. HIV/AIDS • Worldwide as of 2007, 2.5 million children were infected with HIV. • lymphocytes and macrophages contain greatest # of CD4 surface glycoproteins that attach to viral surface proteins (GP120) and enhance host cell invasion and infection. • has a viral enzyme reverse transcriptase that incorporates viral RNA into the host nuclear DNA, leads to death of CD4 cells. • results in opportunistic infections, malignancies (Kaposi sarcoma and lymphoma) and autoimmune diseases.

  38. HIV medical management: • Depends on CD4 count (indicates immune status) and viral load (indicates acceleration of disease). • approximately 30% of newborns of untreated HIV-infected mothers can acquire the HIV virus thru vertical transmission. • Medicating the mother with antiretrovirals such as AZT can decrease rate of transmission by 70%.

  39. Children with HIV: • Only 75% of untreated babies survive to age 5, with 50% of them having severe symptoms. • Clinical findings in infants and children with AIDS are similar to those of adults. • Early manifestations: • interstitial pneumonitis • weight loss • failure to thrive • hepatomegaly and/or splenomegaly • generalized lymphadenopathy • chronic diarrhea. • Also common in children are recurrent and severe bacterial infections.

  40. Oral Manifestations of HIV: Fungal Infections • Candida albicans is most common HIV-associated infection in the mouth. • May lead to esophageal or disseminated candidiasis. • Four oral types of C. albicansare pseudomembranous, hyperplastic, erythematousandangular cheilotic. • Pseudomembranous type: removable creamy white or yellow plaques on palate, buccal mucosa, or dorsum of tongue. Red bleeding surface underneath. • Hyperplastic type: white plaques on buccal mucosa, not easily removed. • Erythematous (atrophic) type: red spotty areas on palate, dorsum of tongueand buccal mucosa. • Angular cheilitis: fissures radiating from commissures of mouth, associated with small white plaques. • Treat all types with topical antifungals (clotrimazole or nystatin) and systemic antifungals (ketoconazole, fluconazole, amphotericin B), and Peridex.

  41. Oral Manifestations of HIV: Viral and Bacterial Infections • HPV: oral warts with raised cauliflower-like appearanceor flat circumscribed look. • HSV: painful ulcerations, most commonly on palate or tongue. • VZV. Oral ulcerations, usually with skin lesions on one side of face. • EBV: Oral hairy leukoplakia shows as white, smooth, corrugated or folded lesion that does not rub off, often on lateral tongue. • Mycobacterium avium-intracellulare and klebsiella pneumonia. • Follow atypical course or unusual response to treatment in HIV pts.

  42. Oral Manifestations of HIV: Neoplasms • Kaposi sarcoma: most common malignancy in AIDS. Intraoral lesions can occur alone or along with skin, visceral and LN lesions. • Red, blue or purple, flat or raised, one or multiple. • Most common oral site is hard palate. • Lymphomas, espNHL. Firm painless swelling in mouth may be first manifestation. Mean survival from time of dx is 6 months. • OSSC also more common in HIV population.

  43. Oral Manifestations of HIV: Idiopathic Lesions • oral ulcers of unknown etiology are increasing in frequency. Appearance is apthous, well-circumscribed with erythematous margins. Sometimes they are large, painful and necrotic. • Salivary gland swelling, usually of parotids, with xerostomia.

  44. Oral Manifestations of HIV: Gingivitis and Periodontitis • May be first sign of HIV infection. No response to standard periodontal therapy. • Rapid progression to advanced disease. Spontaneous bleeding. • Treatment is aggressive curettage, Peridex 3x/day and abx.

  45. Leukemia • proliferation of abnormal leukocytes (blasts) in bone marrow and dissemination of these cells in peripheral bloodand other organs. • Leukemia is classified according to morphology of predominant abnormal WBC in the bone marrow. Can be acute or chronic. • ALL, AML, CML, CLL (not seen in children) • 6550 new cases of cancer dx each year in kids < 15 in U.S. • Acute leukemia is most common malignancy in children.

  46. Leukemia: Clinical Manifestations • Hematopoietic abnormalities: anemia, thrombocytopenia, granulocytopenia. • irritability, lethargy • persistent fever • vague bone pain, easy brusing. • Pallor, petechhiae, cutaneous bruises • tachycardia • adenopathy, hepatosplenomegaly, • gingival bleeding • infections.

  47. Acute Leukemia • 1/3 of all childhood malignancies. • 80% are lymphocytic (ALL). • Chronic leukemia in kids is rare (<2% all cases). • Peak incidence of ALL is b/t age 3-6. • Cause unknown. Radiation, chemical agents, genetics implicated. • Genetic risks: -chromosomal abnormalities (Down Syndrome, Bloom syndrome) -pt with an identical twin with leukemia -some immunologic disorders.

  48. Treatment of Acute Leukemia: • Goal of tx is remission: <5% blasts. • Minimal Residual Disease: <.1% blasts. Better prognosis. • ANLL: < 1 yr of intense tx, with profound bone marrow hypoplasia. • ALL: less intense tx, duration of tx is 2.5-3.5 yrs.

  49. Treatment of Leukemia: Phases • Induction phase: combo of anti-leukemic drugs at staggered intervals for 4 weeks. Maintains regenerative potential of non-malignant hematopoietic cells within the bone marrow. • 95% of ALL pts in remission after 4 weeks. • Consolidation phase: consolidates remission and intensifies prophylactic CNS tx. Intrathecaldose of chemo in lumbar spine has replaced cranial irradiation except for high risk ALL pts. • Interim maintenance: monthly appointment, outpt. Relatively non-toxic agents. • Delayed intensification: to intensive therapy after a short period of less intense therapy. Improves survival for ALL. • Maintenance therapy: 2 yrsfor girls, 3 yrs for boys.

  50. ALL prognosis: • Overall survival of ALL in kids is 80%: • due to improved drugs, combo therapy, radiation, diagnostic techniques, general supportive care. • Those with best response to therapy are between ages 1-10 with a WBC <50,000/cc. • If < 1 yr old or > 10 yrs, EFS is much lower after five years and more intensive treatments needed. • Early response to induction of chemo is strong predictor of outcome for ALL.